a healthy gut

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icecube2
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Candida leaky gut syndrome

Post by icecube2 »

Hi!

I am posting this info again as all my previous posting on Candida seem to have disappeared, and there were quite a few.

Anyways Candida can also cause vitamin deficiency and maybe the cause as to why we are.

I take multi vits myself, and zinc, and those I will continue to take even after I discovered that I had Candida and have since dealt with it.


http://www.leakygut.co.uk/Candidiasis.htm
icecube2
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Re: Candida leaky gut syndrome

Post by icecube2 »

Hi! again,

I forgot to mention, that because I had treated myself to a haircut with my regular hairdresser, who knew nothing of my run in with my good friend Candida, out of the blue, she said she could swear my hair had got thicker, imagine how good that made me feel. Also I noticed my nails have got stronger, so I am now quite accustomed to give them a little file and a splash of varnish now and again.

Thought I'd just say yeah! a bit of useless info for you.

Fiona
icecube2
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Just verification that candida does exist

Post by icecube2 »

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euphoniaa
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Re: Candida leaky gut syndrome

Post by euphoniaa »

icecube2 wrote:Hi!

I am posting this info again as all my previous posting on Candida seem to have disappeared, and there were quite a few.

http://www.leakygut.co.uk/Candidiasis.htm
No, Fiona, as an FYI, your candida posts did NOT disappear from TIMS. :smile: It looks like most of them were moved to the "Natural Approach" forum and incorporated into one of the gigantic combined threads there; most of those posts are on the "Healthy Gut" thread in the Natural Approach Forum.

Here's the link if I copied it right: http://www.thisisms.com/forum/natural-a ... 18577.html

Since you've posted so many threads on the same topic (candida), it seems reasonable to move them to Natural Approach Forum to keep them from filling the entire front page of the General Forum, bumping every other discussion out of view. :smile:

Just my opinion, though.
Dx'd with MS & HNPP (hereditary peripheral neuropathy) 7/03 but must have had MS for 30 yrs before that. I've never taken meds for MS except 1 yr experiment on LDN. (I found diet, exercise, sleep, humor, music help me the most.)
icecube2
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food for thought eh!

Post by icecube2 »

Hi!

The following is a post that I made on my blog in August, I believed it then and I believe in now.

I can assure you will be my last post of the day, I shall now leave you good folk alone. I can hear you breathe a sigh of relief but as Arnie says "I'll be back"
.............................................................................................

Tuesday, 30 August 2011
Ann Boroch and Montel

Ann Boroch was in her twenties and disabled she was diagnosed with ms.

She has A book ok "healing Multiple Sclerosis" which she did through an anti Candida diet removing toxins from her body

Now replace the word "Multiple Sclerosis" from the book title the replace it with "Candida" and it all begins to make sense.

Take a look at u-tube clip and make up your own minds.

Yet again Candida rears its head, is the swank diet similar but without the suppliments that help cause die off of fungus.So like me you can have two thigs going on side by side.

misaligned Atlas + Candida = ms misdiagnosis

and possibly

Lymes + Candida+ ms misdiagnosis or even just Candida =ms misdiagnosis and the list goes on because a lot of Candida symptoms match that of ms.


When is that penny going to drop.
icecube2
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Re: Candida leaky gut syndrome

Post by icecube2 »

Euphoniaa


i suppose that means I have just been educated, didnt realize that one,

the only problem there is that I posted them on General because it is important that everyone is aware of it, because you can have it and just wouldnt know it, I deliberately posted on general because there seems to be a lot of advice given re vitamins and supps, so its only fair people are made aware this could be a reason why.

Not everyone is interested in visiting the natural board, as they dont visit the Antibiotic board, a possible cause, so would never know.

If someone had PMd me and told me, I would have changed my approach, but I was left in the dark, with not a torch to lead my way.

Well you live and learn eh! you live and learn

Fiona
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jimmylegs
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Re: a healthy gut

Post by jimmylegs »

i remember an appointment with my naturopath when i was all gung ho about candida. she said no, no, candida is a secondary infection - but here's this diet plan for ms. i looked at it, then gave her a funny look and said 'but, that's an anti-candida diet!'

so off i went and did my anti-candida thing, but with little success ...until i discovered and corrected the underlying nutritional problems that pre-existed my msdx, i was stuck. zinc turned out to be one of my major problems at that time.

interestingly, the dietary measures my naturopath gave me to consider for ms would yes also counter candida overgrowth, but notably would also help improve zinc status (and a few other things too). this nuance was something it would take me quite some time to realise.

this next post will potentially look a little unfamiliar in this thread, but nonetheless here's me back in the day, trying to be scientific about the candida line of thinking:

http://www.thisisms.com/forum/antibioti ... tml#p16015

now i'm trying to find the post where sarah dissed me over the whole gliotoxin approach - anecdote it was so long ago but can you find it now by chance?? you might remember the words you used better than i... or perhaps could link to the study, or recall the question you referred to david??, on the subject...?

ttfn
JL
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icecube2
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Re: a healthy gut

Post by icecube2 »

JL


I cant be asked, I really cant
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jimmylegs
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Re: a healthy gut

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no probs, you're not sarah.
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Re: a healthy gut

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Shao, Y., Wolf, P. G., Guo, S., Guo, Y., Gaskins, H. R., & Zhang, B. (2017). Zinc enhances intestinal epithelial barrier function through the PI3K/AKT/mTOR signaling pathway in Caco-2 cells. The Journal of Nutritional Biochemistry, 43, 18-26.
http://www.sciencedirect.com/science/ar ... 6316305459

http://www.sciencedirect.com/science/ar ... 6316305459

Zinc plays an important role in maintaining intestinal barrier function as well as modulating cellular signaling recognition and protein kinase activities. The phosphatidylinositol 3-kinase (PI3K) cascade has been demonstrated to affect intercellular integrity and tight junction (TJ) proteins. The current study investigated the hypothesis that zinc regulates intestinal intercellular junction integrity through the PI3K/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway. A transwell model of Caco-2 cell was incubated with 0, 50 and 100 μM of zinc at various time points. Transepithelial electrical resistance (TEER), paracellular permeability, TJ proteins, cell proliferation, differentiation and cell damage were measured. Compared with controls, 50 and 100 μM of zinc increased cell growth at 6, 12 and 24 h and the expression of proliferating cell nuclear antigen at 24 h. Zinc (100 μM) significantly elevated TEER at 6–24 h and reduced TJ permeability at 24 h, accompanied by the up-regulation of alkaline phosphatase (AP) activity and zonula occludens (ZO)-1 expression. In addition, zinc (100 μM) affected the PI3K/AKT/mTOR pathway by stimulating phosphorylation of AKT and the downstream target mTOR. Inhibition of PI3K signaling by LY294002 counteracted zinc promotion, as shown by a decrease in AP activity, TEER, the abundance of ZO-1 and phosphorylation of AKT and mTOR. Additionally, TJ permeability and the expression of caspase-3 and LC3II (markers of cell damage) were increased by addition of PI3K inhibitor. In conclusion, the activation of PI3K/AKT/mTOR signaling by zinc is involved in improving intestinal barrier function by enhancing cell differentiation and expression of TJ protein ZO-1.
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jimmylegs
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Re: a healthy gut

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Bischoff, S. C., Barbara, G., Buurman, W., Ockhuizen, T., Schulzke, J. D., Serino, M., ... & Wells, J. M. (2014). Intestinal permeability–a new target for disease prevention and therapy. BMC gastroenterology, 14(1), 189.
https://bmcgastroenterol.biomedcentral. ... 014-0189-7
full text PDF

Data are accumulating that emphasize the important role of the intestinal barrier and intestinal permeability for health and disease. However, these terms are poorly defined, their assessment is a matter of debate, and their clinical significance is not clearly established. In the present review, current knowledge on mucosal barrier and its role in disease prevention and therapy is summarized. First, the relevant terms ‘intestinal barrier’ and ‘intestinal permeability’ are defined. Secondly, the key element of the intestinal barrier affecting permeability are described. This barrier represents a huge mucosal surface, where billions of bacteria face the largest immune system of our body. On the one hand, an intact intestinal barrier protects the human organism against invasion of microorganisms and toxins, on the other hand, this barrier must be open to absorb essential fluids and nutrients. Such opposing goals are achieved by a complex anatomical and functional structure the intestinal barrier consists of, the functional status of which is described by ‘intestinal permeability’. Third, the regulation of intestinal permeability by diet and bacteria is depicted. In particular, potential barrier disruptors such as hypoperfusion of the gut, infections and toxins, but also selected over-dosed nutrients, drugs, and other lifestyle factors have to be considered. In the fourth part, the means to assess intestinal permeability are presented and critically discussed. The means vary enormously and probably assess different functional components of the barrier. The barrier assessments are further hindered by the natural variability of this functional entity depending on species and genes as well as on diet and other environmental factors. In the final part, we discuss selected diseases associated with increased intestinal permeability such as critically illness, inflammatory bowel diseases, celiac disease, food allergy, irritable bowel syndrome, and – more recently recognized – obesity and metabolic diseases. All these diseases are characterized by inflammation that might be triggered by the translocation of luminal components into the host. In summary, intestinal permeability, which is a feature of intestinal barrier function, is increasingly recognized as being of relevance for health and disease, and therefore, this topic warrants more attention.
not sure why they skipped zinc in the full text section on nutrients.
Michielan, A., & D’Incà, R. (2015). Intestinal permeability in inflammatory bowel disease: pathogenesis, clinical evaluation, and therapy of leaky gut. Mediators of inflammation, 2015.
https://www.hindawi.com/journals/mi/2015/628157/abs/
Butyrate, zinc, and some probiotics also ameliorate mucosal barrier dysfunction but their use is still limited and further studies are needed before considering permeability manipulation as a therapeutic target in IBD.
Tran, C. D., Hawkes, J., Graham, R. D., Kitchen, J. L., Symonds, E. L., Davidson, G. P., & Butler, R. N. (2015). Zinc-fortified oral rehydration solution improved intestinal permeability and small intestinal mucosal recovery. Clinical pediatrics, 54(7), 676-682.
http://journals.sagepub.com/doi/abs/10. ... 2814562665
A randomized double-blind placebo-controlled study was conducted in children admitted to hospital with gastroenteritis (≥3 loose stools per day). All were treated for 5 days following admission with either zinc (Zn, 3 mg) or without Zn-fortified rice-based oral rehydration solution (ORS). 13C-sucrose breath test (SBT) and intestinal permeability (lactulose/rhamnose or L/R ratio) were performed concurrently prior to commencement of ORS with or without Zn and at day 5 post-admission. There was a significant improvement in the SBT results in both the Zn-fortified group, median (5th-95th percentile) 2.1% (0.4% to 8.3%) versus 4.4% (0.4% to 10.4%), P < .05, and control group, 1.4% (0.1% to 5.4%) versus 4.3% (0.4% to 11.4%), P < .05, between the day of admission and day 5 post-admission. In the Zn-fortified group, there was also a significant improvement in L/R ratio between the day of admission and day 5 post-admission, 53.0 (19.5-90.6) versus 17.7 (13.4-83.2), P < .05. Low levels of Zn improved intestinal permeability but did not enhance short-term recovery following diarrheal illness.
might not have been enough - nephews get 8mg per day in their childrens' gummie supplement.

will be a related good read when i have more time: Suzuki, T. (2013). Regulation of intestinal epithelial permeability by tight junctions. Cellular and molecular life sciences, 70(4), 631-659.
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jimmylegs
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Re: a healthy gut

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The Impact of Diet and Lifestyle on Gut Microbiota and Human Health
free full text: http://www.mdpi.com/2072-6643/7/1/17/htm
Abstract: There is growing recognition of the role of diet and other environmental factors in modulating the composition and metabolic activity of the human gut microbiota, which in turn can impact health. This narrative review explores the relevant contemporary scientific literature to provide a general perspective of this broad area. Molecular technologies have greatly advanced our understanding of the complexity and diversity of the gut microbial communities within and between individuals. Diet, particularly macronutrients, has a major role in shaping the composition and activity of these complex populations. Despite the body of knowledge that exists on the effects of carbohydrates there are still many unanswered questions. The impacts of dietary fats and protein on the gut microbiota are less well defined. Both short- and long-term dietary change can influence the microbial profiles, and infant nutrition may have life-long consequences through microbial modulation of the immune system. The impact of environmental factors, including aspects of lifestyle, on the microbiota is particularly poorly understood but some of these factors are described. We also discuss the use and potential benefits of prebiotics and probiotics to modify microbial populations. A description of some areas that should be addressed in future research is also presented.
omgomgomg yay for the nasa connection :D :D :D #spacefan actually as close as i think i will ever get to being a #fangirl over anything
The Integrated Impact of Diet On Human Immune Response, the Gut Microbiota, and Nutritional Status During Adaptation to a Spaceflight Analog
https://ntrs.nasa.gov/search.jsp?R=20170000370
Spaceflight impacts human physiology, including well documented immune system dysregulation. Diet, immune function, and the microbiome are interlinked, but diet is the only one of these factors that we have the ability to easily, and significantly, alter on Earth or during flight. As we understand dietary impacts on physiology more thoroughly, we may then improve the spaceflight diet to improve crew health and potentially reduce flight-associated physiological alterations. It is expected that increasing the consumption of fruits and vegetables and bioactive compounds (e.g.,omega-3 fatty acids, lycopene, flavonoids) and therefore enhancing overall nutritional intake from the nominal shelf-stable, fully-processed space food system could serve as a countermeasure to improve human immunological profiles, the taxonomic profile of the gut microbiota, and nutritional status, especially where currently dysregulated during spaceflight. This interdisciplinary study will determine the effect of the current shelf-stable spaceflight diet compared to an "enhanced" shelf-stable spaceflight diet (25% more foods rich in omega-3 fatty acids, lycopene, flavonoids, fruits, and vegetables). The NASA Human Exploration Research Analog (HERA) 2017 missions, consisting of closed chamber confinement, realistic mission simulation, in a high-fidelity mock space vehicle, will serve as a platform to replicate mission stressors and the dysregulated physiology observed in astronauts. Biosampling of crew members will occur at selected intervals, with complete dietary tracking. Outcome measures will include immune markers (e.g., peripheral leukocyte distribution, inflammatory cytokine profiles, T cell function), the taxonomic and metatranscriptomic profile of the gut microbiome, and nutritional status biomarkers and metabolites. Data collection will also include complete dietary tracking. Statistical evaluations will determine physiological and biochemical shifts in relation to nutrient in take and study phase. Beneficial improvements will provide evidence of the impact of diet on crew health and adaptation to this spaceflight analog, and will aid in the design and development of more-efficient targeted dietary interventions.
eeeeeeeeeeeee
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jimmylegs
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Re: a healthy gut

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Gut bacteria from multiple sclerosis patients modulate human T cells and exacerbate symptoms in mouse models
http://www.pnas.org/content/114/40/10713.abstract
Abstract
The gut microbiota regulates T cell functions throughout the body. We hypothesized that intestinal bacteria impact the pathogenesis of multiple sclerosis (MS), an autoimmune disorder of the CNS and thus analyzed the microbiomes of 71 MS patients not undergoing treatment and 71 healthy controls. Although no major shifts in microbial community structure were found, we identified specific bacterial taxa that were significantly associated with MS. Akkermansia muciniphila and Acinetobacter calcoaceticus, both increased in MS patients, induced proinflammatory responses in human peripheral blood mononuclear cells and in monocolonized mice. In contrast, Parabacteroides distasonis, which was reduced in MS patients, stimulated anti-inflammatory IL-10–expressing human CD4+CD25+ T cells and IL-10+FoxP3+ Tregs in mice. Finally, microbiota transplants from MS patients into germ-free mice resulted in more severe symptoms of experimental autoimmune encephalomyelitis and reduced proportions of IL-10+ Tregs compared with mice “humanized” with microbiota from healthy controls. This study identifies specific human gut bacteria that regulate adaptive autoimmune responses, suggesting therapeutic targeting of the microbiota as a treatment for MS.
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jimmylegs
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Re: a healthy gut

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hmm looks like this one is gonna take some reading... how high is high in MS? how low is low in obesity?

Akkermansia muciniphila and improved metabolic health during a dietary intervention in obesity: relationship with gut microbiome richness and ecology
http://gut.bmj.com/content/early/2015/0 ... 8778.short

Abstract
Objective Individuals with obesity and type 2 diabetes differ from lean and healthy individuals in their abundance of certain gut microbial species and microbial gene richness. Abundance of Akkermansia muciniphila, a mucin-degrading bacterium, has been inversely associated with body fat mass and glucose intolerance in mice, but more evidence is needed in humans. The impact of diet and weight loss on this bacterial species is unknown. Our objective was to evaluate the association between faecal A. muciniphila abundance, faecal microbiome gene richness, diet, host characteristics, and their changes after calorie restriction (CR).

Design The intervention consisted of a 6-week CR period followed by a 6-week weight stabilisation diet in overweight and obese adults (N=49, including 41 women). Faecal A. muciniphila abundance, faecal microbial gene richness, diet and bioclinical parameters were measured at baseline and after CR and weight stabilisation.

Results At baseline A. muciniphila was inversely related to fasting glucose, waist-to-hip ratio and subcutaneous adipocyte diameter. Subjects with higher gene richness and A. muciniphila abundance exhibited the healthiest metabolic status, particularly in fasting plasma glucose, plasma triglycerides and body fat distribution. Individuals with higher baseline A. muciniphila displayed greater improvement in insulin sensitivity markers and other clinical parameters after CR. These participants also experienced a reduction in A. muciniphila abundance, but it remained significantly higher than in individuals with lower baseline abundance. A. muciniphila was associated with microbial species known to be related to health.

Conclusions A. muciniphila is associated with a healthier metabolic status and better clinical outcomes after CR in overweight/obese adults. The interaction between gut microbiota ecology and A. muciniphila warrants further investigation.
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jimmylegs
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Re: a healthy gut

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Diet Affects Gut Microbiota and Modulates Hospitalization Risk Differentially In an International Cirrhosis Cohort (2018)
https://aasldpubs.onlinelibrary.wiley.c ... /hep.29791

Abstract
The relative ranking of cirrhosis‐related deaths differs between high/middle‐income countries. Gut microbiome is affected in cirrhosis and related to diet. Our aim was to determine the effect of differing dietary habits on gut microbiota and clinical outcomes.

Methods: Outpatient compensated/decompensated cirrhotics and controls from Turkey and USA underwent dietary and stool microbiota analysis. Cirrhotics were followed till 90‐day hospitalizations. Shannon diversity and multi‐variable determinants (Cox and binary logistic) of microbial diversity and hospitalizations were studied within/between groups.

Results: 296 subjects (157 USA:48 controls, 59 compensated, 50 decompensated, 139 Turkey:46 controls, 50 compensated, 43 decompensated) were included. Cirrhotics between cohorts had similar MELD scores. American cirrhotics had more men, greater rifaximin/lactulose use and higher hepatitis C/alcohol etiologies. Coffee intake was higher in Americans while tea, fermented milk and chocolate intake were higher in Turkey. The entire Turkish cohort had a significantly higher diversity than Americans, which did not change between their controls and cirrhotics. In contrast, diversity changed in the US‐based cohort and was the lowest in decompensated patients. Coffee, tea, vegetable, chocolate and fermented milk intake predicted a higher diversity while MELD score, lactulose use and carbonated beverage use predicted a lower microbial diversity. The Turkish cohort had a lower risk of 90‐day hospitalizations. On Cox and binary logistic regression, microbial diversity was protective against 90‐day hospitalizations, along with coffee/tea, vegetable and cereal intake.

Conclusions: In this study of cirrhotic patients and healthy controls from USA and Turkey, a diet rich in fermented milk, vegetables, cereals, coffee and tea, is associated with a higher microbial diversity. Microbial diversity was associated with an independently lower risk of 90‐day hospitalizations.

*****

interp caveat - 'diet rich in' does not suggest 'exclusively' the above or 'to the exclusion of' other healthful foods and drinks.
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